心脏成纤维细胞缺氧预处理对心肌细胞的保护作用

目的 :探讨大鼠心脏成纤维细胞缺血预处理 (IPC)对成纤维细胞及心肌细胞的保护作用。方法 :实验分为 6组 [对照 (CON) 1组、CON 2组 ,预处理 (PC) 1组、PC 2组、SMT组、NS3 98组 )。用Westernblotting法测定心肌细胞的环氧化酶 2 (COX2 )、分泌型一氧化氮合酶 (iNOS)表达量。心肌细胞损伤程度以乳酸脱氢酶 (LDH)释放和台盼蓝排斥试验判断 ,成纤维细胞损伤程度以台盼蓝排斥试验判断。结果 :PC 1组的细胞存活率与CON1组差异无显著性意义 (P >0 .0 5 )。PC2组LDH释放较CON2组明显减少 ,细胞存活率明显增加 (P <0 .0 1)。SMT组和NS3 98组LDH释放、细胞存活率与CON2组相当 (P >0 .0 5 )。PC2组COX2 表达量明显增加 ,与CON2组比较差异有极显著性意义 (P <0 .0 1) ,SMT组与CON2组间COX2 量差异无显著性意义 (P >0 .0 5 )。PC2组和NS3 98组的iNOS表达量较CON2组明显增加 ,差异有极显著性意义 (P <0 .0 1)。结论 :IPC不能对心脏成纤维细胞产生保护作用。心脏成纤维细胞在缺氧后可能释放某些“保护性递质” ,触发心肌细胞产生类似IPC的保护效应 ,而且与iNOS ,COX2 的表达有关 ,在信号传导中iNOS是COX2 的上游

The cardioprotective effect of the ischemic preconditioning of rat cardiac fibroblast

Objective: To explore the protective effects of ischemic preconditioning in rat cardiac fibroblast on cardiac fibroblast and cardiomyocyte. Methods: The expression of COX 2 and iNOS were determinated by western blotting techniques and the injury of cardiomyocyte was assessed by LDH release and trypan blue exclusion , the injury of cardiac fibroblast was assessed by trypan blue exclusion in six groups(n=4 in each)-Group control-1, Group control-2,Group PC-1, Group PC-2,Group SMT and Group NS 398. Results: The difference of cell viability was not significant between Group control-1 and Group PC-1(P> 0.05). The LDH was lower ,and cell viability was higher in Group PC-2 than Group control-2(P< 0.01). The difference of the LDH and cell viability was not significant among Group control-2 ,Group SMT and Group NS 398(P> 0.05). The expression of COX 2 in Group PC-2 increased markedly in comparision with Group control-2(P< 0.01). The difference of the amount of COX 2 was not significant between Group SMT and Group control-2(P> 0.05). The expression of iNOS in Group PC-2 and Group NS398 was higher than Group control-2(P< 0.01). The difference of the amount of iNOS was not significant between Group PC-2 and Group NS398(P> 0.05). Conclusion: Ischemic preconditioning do not protect cardiac fibroblasts from the lethal injury of the ischemia. After the stimulus of the brief ischemia,the cardiac fibroblasts may release 'protective factor' and trigger the protective effect on cardiomycytes,which is associated with the expression of iNOS and COX2 in cardiomycytes, and increase iNOS may be an upstream of COX 2 in signal transduction.